The present invention relates to improvements in artificial optical lenses such as contact lenses, intraocular lenses and intracorneal implants, and, more particularly to such optical lenses having an outermost surface of modified morphology to provide improved biological inertness.
It has been postulated that the interaction of an implant surface of an optical lens with surrounding biological tissue which results in bacterial colonization and tissue integration adjacent the implant is controlled by long range attractive hydrophobic interactions which extend outward from the implant surface a distance up to 300 Angstroms. See for example Gristina, A., "Biomaterial-Centered Infection: Microbial Adhesion Versus Tissue Integration," Science, Vol. 237, pp. 1588. Such long range attractive hydrophobic interactions may be attributed to changes in entropy associated with disruption of the supramolecular structure of water molecules in liquid water at the implant surface immersed in an aqueous medium. The precise molecular structure of the implant surface and its interaction with its environment determines the energetics of electrostatic or exchange interactions. However, the undesired long range attractive hydrophobic interactions cannot be effected by changing electrostatic or exchange interactions at the implant surface since such interactions are short range in character and rarely extend beyond 20 Angstroms from the surface. Therefore, changes in the molecular structure of an implant surface are inadequate to prevent inflammatory reactions or tissue irritation commonly associated with optical lens implants.
As distinguished from attempts to reduce inflammatory reactions and tissue irritations by changing electrostatic or exchange interactions at an implant surface, I have discovered a surface passivation process which when applied to an acrylic polymer optical lens, forms a surface of reduced energy and high biological inertness. Such optical lenses have been found to possess superior anti-inflammatory and minimal tissue irritation qualities. The low surface energy associated with my surface passivation process is achieved by removing molecular level irregularities from the surface of the optical lens resulting in a smooth passivated surface layer with minimum interaction with biological tissue. More particularly, I have found that the morphology of the implant surface of an optical lens controls the increase in entropy and consequently the overall free energy associated with the destruction of the highly organized structure of hydrogen bonded oligomers of water molecules existing in liquid water at an implant surface immersed in an aqueous medium. When a tissue or a biomolecule approaches the implant surface of my surface passivated optical lens immersed in an aqueous medium, water molecules which have been displaced from their stable position by the implant surface interact with the tissue surface of the biomolecule. Such interaction provides an additional site for the development of hydrogen bonded intermolecular structures. This leads to a decrease in the entropy and the free energy of the system which comprises the implant surface, the surrounding aqueous medium, and the approaching biological material.